ECE2021 Audio Eposter Presentations Pituitary and Neuroendocrinology (113 abstracts)
Treatment regimens affecting glucose metabolism and gastrointestinal hormones in acromegaly: A descriptive study
Nanna Jørgensen 1 , Trine Erichsen 1 , Marianne Klose 1 , Morten Joergensen 2 , Thomas Idorn 2 , Bo Feldt-Rasmussen 2 , Jens J. Holst 3 & Ulla Feldt-Rasmussen 1
1Department of Endocrinology, Copenhagen University Hospital, Rigshospitalet, Denmark; 2Department of Nephrology, Copenhagen University Hospital, Rigshospitalet, Denmark; 3Department of Biomedical Sciences, and NNF Centre for Basic Metabolic Research Faculty of Health Science, Copenhagen University, Denmark
Context
Active acromegaly is associated with impaired glucose metabolism, which improves upon treatment. Treatment options include surgery, medical therapy with somatostatin analogues (SSA) and Pegvisomant (PEG) and in few cases irradiation.
Objective
To describe the differential effect of various treatment regimens on the secretion of glucose, insulin, glucagon, glucagon-like peptide-1 (GLP1), and glucose-dependent insulinotropic polypeptide (GIP) in patients with acromegaly.
Methods
Descriptive study of data from 23 surgically treated, non-diabetic patients with acromegaly and 12 healthy controls. Participants underwent an oral glucose tolerance test (OGTT) and subsequently isoglycaemic intravenous glucose infusion on a separate day, both with continuous measurement of the above-mentioned hormones. Analysis: Baseline hormone concentrations, time-to-peak and area under the curve (AUC) on the OGTT-day. Groups were compared using ANOVA.
Results
The patients treated with SSA (N=15) had impaired insulin, glucagon, GLP1 and GIP-response (AUC, P=0.007), and numerical impairment of all other hormone responses (AUC, P>0.05)(Table 1). Patients co-treated with pegvisomant (SSA+PEG, N=4) had a numerically increased secretion of insulin and glucagon compared to patients only treated with SSA (N=11) (insulin AUC mean (SEM), SSA+PEG 49 nmol/l*min (8.3) vs SSA%PEG 25 (3.4), P>0.05); glucagon AUC, SSA+PEG 823 pmol/l*min (194) vs SSA%PEG 332 (69), P>0.05). GIP secretion remained significantly impaired, whereas GLP1 secretion was numerically increased with PEG (SSA+PEG 3088 pmol/l*min (366) vs mono-SSA 2401 (239), P>0.05) (Table 1). Similarly, the incretin-effect was numerically increased in SSA+PEG compared to SSA%PEG. No difference was found between patients treated with/without radiotherapy nor substituted or not with hydrocortisone.
| Controls | SSA%PEG | SSA+PEG | P | |
| N | 6 | 11 | 4 | - |
| Glucose-AUC (mmol/l*min) | 1352 (78) | 1487 (62) | 1508 (109) | 0.1 |
| Insulin-AUC (nmol/l*min) | 62 (14) | 25 (3) | 49 (8) | 0.006a |
| Glucagon-AUC (pmol/l*min) | 946 (233) | 332 (69) | 823 (194) | 0.01a |
| GLP1-AUC (pmol/l*min) | 3972 (451) | 2401 (239) | 3088 (366) | 0.007a |
| GIP-AUC (pmol/l*min) | 11062 (2334) | 2658 (356) | 2237 (240) | 0.0001a/0.001b |
| Incretin effect (%) | 55.5% (7.7) | 33.6% (47.4) | 49.9% (13.9) | |
| Results are mean (SEM). Analyses by one-way ANOVA with post-hoc analysis. aSSA%PEG compared to controls, bSSA+PEG compared to controls | ||||
Conclusion
SSA impaired the insulin, glucagon and incretin hormones secretion. Co-treatment with Pegvisomant seemed to counteract the somatostatinergic inhibition of the glucagon secretion and improved the insulin response to OGTT. We speculate that Pegvisomant exerts its action via GH-receptors on pancreatic δ-cells.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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